KRAS and neoplasm: Continuous treatment with KRAS G12C inhibitors could result in copy‐number gain of the KRAS G12C allele and positive selection of resistant KRAS mutations, leading to tumor rebound.[33] Pan‐KRAS degraders and multi‐RAS inhibitors will likely be susceptible to resistance mechanisms that cause reactivation of ERK signaling.[11, 12] However, the bedside data for adaptive resistance after multi‐RAS inhibition or pan‐KRAS degradation are currently scare and pending further disclosure.